CHN1 as a Predictive Biomarker for Atopic Dermatitis-related Depression

The comorbidity of Atopic Dermatitis (AD) and depression has garnered increasing attention in recent years. Yet, the immunopathological mechanisms underlying this connection remain unclear. To bridge this gap, we collected peripheral blood mononuclear cell samples from 20 AD patients with and without depression, and performed RNA sequencing analysis. By integrating bioinformatics and machine learning techniques, we aimed to uncover the immune regulatory networks and identify key genetic markers for the depression comorbidity in AD patients. Our analysis revealed 394 differentially expressed genes in AD patients with depression as compared to those non-depression counterparts. Weighted gene co-expression network analysis pinpointed a pink module encompassing 83 genes strongly linked to depression. Functional enrichment analysis of critical module genes revealed significant enrichment scores in neurotransmitter uptake and the negative regulation of T-helper (Th) 17 cell differentiation. Furthermore, machine learning models of least absolute shrinkage and selection operator and support vector machines highlighted CHN1 as a potential pivotal gene upregulated in AD patients with depression. The expression level of CHN1 demonstrated positive correlation with Th2 and Th17 cytokine families, as well as with the Hospital Anxiety and Depression Scale-Depression score and Eczema Area and Severity Index. Validation experiments on clinical samples of an additional 20 participants confirmed the significant upregulation of CHN1 in depressed AD patients. This study is the first to unveil the intricate inflammatory and immune pathways underlying AD-associated depression, shedding light on the critical role of CHN1 connecting inflammation and neuropsychiatric symptoms. Overall design: We collected peripheral blood mononuclear cell samples from 20 AD patients with (DAD) and without depression (NAD), and performed RNA sequencing analysis.